Bottom Line:
The elevated intraocular pressure was considered the prime factor responsible for the glaucomatous optic neuropathy involving death of retinal ganglion cells and their axons.A better understanding of the pathophysiological mechanisms involved in the onset and progression of glaucomatous optic neuropathy is crucial in the development of better therapeutic options.The literature available in the National Medical Library and online Pubmed search engine was used for literature review.

ABSTRACTGlaucoma, the second leading cause of blindness, is characterized by changes in the optic disc and visual field defects. The elevated intraocular pressure was considered the prime factor responsible for the glaucomatous optic neuropathy involving death of retinal ganglion cells and their axons. Extensive investigations into the pathophysiology of glaucoma now reveal the role of multiple factors in the development of retinal ganglion cell death. A better understanding of the pathophysiological mechanisms involved in the onset and progression of glaucomatous optic neuropathy is crucial in the development of better therapeutic options. This review is an effort to summarize the current concepts in the pathophysiology of glaucoma so that newer therapeutic targets can be recognized. The literature available in the National Medical Library and online Pubmed search engine was used for literature review.

Mentions:
Nakazawa et al., have now demonstrated rapid upregulation of TNF-A in rats with experimentally induced elevated IOP and this was followed sequentially by microglial activation, loss of optic nerve oligodendrocytes, and delayed loss of RGCs.[46] An upregulation of TNF-A in the astrocytes was also detected in human glaucomatous optic nerve head and this expression was found to parallel the progression of neurodegeneration. TNF-A stimulation seems to contribute to neuronal damage by both a direct effect on the axons of the RGCs and by inducing nitric oxide synthase (NOS)-2 in astrocytes.[47] A summary of mechanisms involved in RGC apoptosis secondary to elevated IOP is presented in Fig. 1.

Mentions:
Nakazawa et al., have now demonstrated rapid upregulation of TNF-A in rats with experimentally induced elevated IOP and this was followed sequentially by microglial activation, loss of optic nerve oligodendrocytes, and delayed loss of RGCs.[46] An upregulation of TNF-A in the astrocytes was also detected in human glaucomatous optic nerve head and this expression was found to parallel the progression of neurodegeneration. TNF-A stimulation seems to contribute to neuronal damage by both a direct effect on the axons of the RGCs and by inducing nitric oxide synthase (NOS)-2 in astrocytes.[47] A summary of mechanisms involved in RGC apoptosis secondary to elevated IOP is presented in Fig. 1.

Bottom Line:
The elevated intraocular pressure was considered the prime factor responsible for the glaucomatous optic neuropathy involving death of retinal ganglion cells and their axons.A better understanding of the pathophysiological mechanisms involved in the onset and progression of glaucomatous optic neuropathy is crucial in the development of better therapeutic options.The literature available in the National Medical Library and online Pubmed search engine was used for literature review.

ABSTRACTGlaucoma, the second leading cause of blindness, is characterized by changes in the optic disc and visual field defects. The elevated intraocular pressure was considered the prime factor responsible for the glaucomatous optic neuropathy involving death of retinal ganglion cells and their axons. Extensive investigations into the pathophysiology of glaucoma now reveal the role of multiple factors in the development of retinal ganglion cell death. A better understanding of the pathophysiological mechanisms involved in the onset and progression of glaucomatous optic neuropathy is crucial in the development of better therapeutic options. This review is an effort to summarize the current concepts in the pathophysiology of glaucoma so that newer therapeutic targets can be recognized. The literature available in the National Medical Library and online Pubmed search engine was used for literature review.